MicroRNAs are single-stranded RNA molecules that are 21-23 nucleotides in length (Wienholds, 2005). Several hundred miRNAs have been identified in plants, animals and viral RNA genomes (Bartel, 2004; Liu et al., 2005). In animals, miRNAs regulate many cellular processes by binding to 3′-UTRs of their target mRNAs, causing translational repression of the target mRNA (Bartel, 2004). Recent studies showed that viral miRNAs play an important role in regulating viral infection in host cells by targeting the cellular or viral genes. Viral miRNAs are capable of controlling expression of viral or cellular genes.
Cellular miRNAs can regulate viral infections. Host-derived miR-24 and miR-93 have been found to target the VSV large protein (L protein) and phosphoprotein (P protein) genes, respectively. A deficiency in miR-24 and miR-93 was responsible for increased vesicular stomatitis virus (VSV) propagation in Dicer1 knockout cells (Otsuka et al., 2007). Furthermore, Lecellier et al. reported that host miR-32 effectively inhibits the accumulation of the retrovirus primate foamy virus type 1 (PFV-1) in human cells by targeting a sequence in the genome of the PFV-1 (Lecellier et al., 2005). Huang et al. reported that a cluster of cellular miRNAs, including miR-28, miR-125b, miR-150, miR-223 and miR-382, targets the 3′ ends of various human immunodeficiency virus 1 (HIV-1) mRNAs. These host miRNAs are enriched in resting CD4+ T cells as compared to activated CD4+ T cells, indicating that these cellular miRNAs are important to maintain HIV-1 latency (Huange et al., 2007). Inhibition of miR-122, a cellular miRNA highly and specifically expressed in the human liver, resulted in a marked loss in autonomous replication of hepatitis C viral RNAs, suggesting that miR-122 likely enhances propagation of the virus (Chang et al., 2008; Jopling et al., 2005).